are presented as metabolism-linked regulators and possible therapeutic targets in .
Evidence
This review synthesizes mechanistic and preclinical evidence on SIRT1-SIRT7 pathways and sirtuin-targeting strategies in renal fibrosis models.
Caveat
Clinical translation remains uncertain because effects may vary by cell type and disease stage, and selective renal-targeted modulators are still needed.
Simplified
represents the common pathological endpoint of chronic kidney disease (CKD) progression, yet effective therapies remain limited. The family (SIRT1-SIRT7), NAD-dependent deacetylases, functions as a critical molecular hub linking metabolism, stress responses, and homeostasis. This review systematically delineates the integrated anti-fibrotic mechanisms of sirtuins: SIRT1, SIRT3, and SIRT6 suppress TGF-β/Smad and Wnt/β-catenin signaling; activate the AMPK/PGC-1α axis to correct metabolic dysregulation; promote autophagyFoxO and TFEB; and alleviate oxidative stress and inflammation through Nrf2 and NF-κB modulation. We further summarize diverse therapeutic strategies targeting sirtuins-including natural compounds, traditional Chinese medicine formulations, synthetic drugs, gene therapy, bioactive peptides, and exercise training-that exhibit significant anti-fibrotic efficacy in preclinical models. Despite promising evidence, clinical translation faces challenges including cell-type-specific functional duality, disease-stage-dependent effects, and the need for highly selective modulators with improved bioavailability and renal targeting. This review highlights sirtuins as a multi-dimensional regulatory network and a promising therapeutic frontier in renal fibrosis, while outlining key obstacles and future directions for clinical application. + via
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